Rheumatoid Arthritis Presentation

8/7/2019 Rheumatoid Arthritis Presentation

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Prepared by:

ASYA'ARI BIN ARIF

RASHEEDI JUZAIMIE BIN JUSOH

MUHAMMAD AFIQ BIN MOHD RAZALI

NUR NADIATUL NABILA BT AHMAD SAIFUDDIN

RHEUMATOID

ARTHRITIS


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DEFINITION

RA is a systemic , chronic

inflammation disease affecting many

tissues

principally attacking the joints toproduce nonsuppurative proliferative

synovitis

3 to 5 times more common in women

than men

peak incidence : 2nd to 4th decades of

life


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EPIDEMIOLOGYAND HISTORY

Gender Women are two-to-three times more likely than men to develop

rheumatoid arthritis. The exact cause for this is not known, but

it may be related to the hormone, oestrogen

Age

Rheumatoid arthritis can develop at any age but it is more

common in older people. It is most likely to be diagnosed in

people between 40 and 60 years of age

.

Family history

Although rheumatoid arthritis is not a hereditary disease,certain genes can make a person more susceptible to it. This

means that people with close relatives who suffer from

rheumatoid arthritis have a higher than usual risk of developing

it themselves because they may have inherited the same

genes. However, they are still more likely not to get the disease

than to get it.


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.

Family history

Although rheumatoid arthritis is not a hereditary disease,

certain genes can make a person more susceptible to it.

This means that people with close relatives who suffer fromrheumatoid arthritis have a higher than usual risk of

developing it themselves because they may have inherited

the same genes. However, they are still more likely not to

get the disease than to get it.

Smoking

People who smoke have a higher risk of developing

rheumatoid arthritis than those who do not.

Picture of people of different races

In Europe and North America, rheumatoid arthritis affects

0.51% of the population in total. However, it is much more

common in Native Americans (affecting over 5%) and less

common in African and Asian people. This suggests that

there are genetic factors involved in the development of the

disease.


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CAUSES

The cause of rheumatoid arthritis is unknown.

Even though infectious agents such as

viruses, bacteria, and fungi have long been

suspected, none has been proven as the cause

It is believed that the tendency to develop

rheumatoid arthritis may be genetically

inherited

Environmental factors also seem to play some

role in causing rheumatoid arthritis. For

example, scientists have reported that smoking

tobacco increases the risk of developingrheumatoid arthritis.


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MORPHOLOGY

A)Articular Lesion

The most severe form

Present as symmetric arthritis,affect small joint of

hand,feet,ankle,knees,wrists,elbows and

shoulders.

Typical in proximal interphalangeal and

metacarpophalangeal

Frequent in cervical spine


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1. Joint

- synovium becomes grossly edematous, thickened and

hyperplastic(bulbous fronds)

-Histologic features:

i. Dense perivascular inflammatory cell infiltrate(form

lymphoid follicle) in synovium composed of CD4+ T Cell,

B cell,plasma cell,dendritic cells and macrophage.

ii. Increased vascularity due to angiogenesis and

vasodilation.

iii. Aggregation of organizing fibrin on synovial surface and

float in joint space as rice bodies

iv. Accumulation of neutrophils in synovial fluids and along

synovium surface.

v. Increased osteoclast activity in the underlying

bones,leading to synovial penetration and bone erosion.

vi. Pannus formation


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Villous hypertrophy of the synovium is seen, forming large papillary projections

on the surface. These are characterized by proliferation of the synoviocytes and

aggregates of inflammatory cells within the villous stroma.


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At higher magnification ,subsynovial

tissue containing a dense lymphoid

aggregate is seen


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The region of the synovial lining that erodes into the bone, which is known as the pannus,

contains macrophages, fibroblasts and osteoclasts, which contribute to the cartilage and bone

destruction76. The sublining region of the rheumatoid joint is replete with blood vessels, which

are important for delivering inflammatory cells to the joint, such as monocytes and lymphocytes.


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B)Extra-Articular Lesion

Nonspecific inflammatory changes seen in bloodvessels(acute vasculitis) , lung

,pleura,pericardium,myocardium,lymph

nodes,peripheral nerves and eyes.


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1. Skin (rheumatoid nodules)

Most common cutaneous lesion

Arise in region of the skin that are subjected

to pressure,including the ulnar aspect of the

forearm,elbows,occiput and lumbosacral area.

Less common form in the

lungs,spleen,pericardium,myocardium,heart

valves,aorta and other viscera.

Microscopically: the centre of nodule consist

of area of fibrinoid necrosis surrounded by a

prominent rim of epithelioid

histiocytes(activated macrophage) and

numerous lymphocytes and plasma cells.


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A closer view showing the central necrosis on the left

side of the photomicrograph, with successive layers of

palisading macrophages and lymphocytes (to the right

of the necrosis).

Necrotizing granuloma surrounded by palisading histiocytes

and foreign body giant cell (black arrow)


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Rheumatoid Nodules. Rheumatoid nodules commonly form near the extensor surface

of the elbow. They can be fixed to the underlying periosteum or can be freely mobile


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2. Blood Vessels (Rheumatoid vasculitis)

Developed in high risk in affected individuals with

severe erosive disease, rheumatoid nodules and

high titers of rheumatoid factors .

Characterized by inflammatory destruction of small

and medium-sized blood vessels primarily due to leukocyte migration and resultant

damage.

Development of red spots on the skin as a result.


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PATHOGENESIS

-The joint inflammation is immunologically mediated

- The initiating agent/s are not yet understood- Proposed that it is initiated by activation ofCD4+ helper

T cells

- The activated T cells produce cytokines that :-

a)A

ctivate macrophages and other cells in the jointspace, releasing degenerative enzymes and other

factors that perpetuate inflammation..

b) Activate B cells, resulting in the production of

antibodies, some of which are directed against self-

antigens in the joint.

- The rheumatoid synovium is rich in both lymphocytes-

and-macrophage-derived cytokines.

- Activated T cells in RA lesions have also been shown

to express impressive amounts of cytokine called

RANKligand .


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The role of antibodies in the disease is suspected

from a variety of experimental and clinicalobservations .

About 80% of patients have serum IgM ( and less

frequently IgG ) autoantibodies that bind to the Fc

portions of their own (self) IgG

These autoantibodies are called rheumatoid factor (RF )

Genetic variables in the pathogenesis ofRA are

suggested by the increased frequency of this disease

among first-degree relatives and a high concordance

rate in monozygotic twins

There are also associations of HLA DR4 and

polymorphism in the PTPN22 gene with RA

There are elusive infectious agents whose antigens

may activate T or B cells.


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Articular surface (top) shows loss of articular cartilage

beneath pannus overgrowth


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The inflammation associated with RA can lead to

fibrosis (arrow) and fusion of the joint (ankylosis)


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SYMPTOMS & SIGNS

Come & go.

Primarily affects joints, others are known

When active several symptoms can be

acknowledged

- fatigue

- loss of energy

- lack of appetite

- muscle and joint aches

- stiffness

During flares- joints frequently become red,

swollen, painful, and tender.


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In rheumatoid arthritis, multiple joints are usually

inflamed in a symmetrical pattern

Occasionally, only one joint is inflamed.

Chronic inflammation can cause damage to body

tissues, including cartilage and bone.

is a systemic disease, its inflammation can affect

organs and areas of the body other than the joints.


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DIAGNOSIS

Imaging x rays, ultrasound,MRI Stage I

no damage seen on X-rays, although there may be signs of

bone thinning

Stage II on X-ray, evidence of bone thinning around a joint with or

without slight bone damage

abnormalities of soft tissue around joint possible


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Stage III

on X-ray, evidence of cartilage and bone

damage and bone thinning around the joint

joint deformity without permanent stiffening orfixation of the joint

extensive muscle atrophy

abnormalities of soft tissue around joint

possible

Stage IV

on X-ray, evidence of cartilage and bone

damage and osteoporosis around joint

joint deformity with permanent fixation of the

joint

extensive muscle atrophy

abnormalities of soft tissue around jointpossible

Blood test

rheumatoid factor

sedimentation rate


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TREATMENT

First-line medication

NSAIDs

NSAIDs are medications that can reduce tissue

inflammation, pain, and swelling

NSAIDs have side effects

Example ofNSAIDs aspirin (acetylsalicylate)

Corticosteroid medications

more potent than NSAIDs

useful for short periods during severe flares of

disease activity or when the disease is not

responding to NSAIDs

Have serious side


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Second-line or "slow-acting" drugs

Disease-modifying anti-rheumatic drugs or

DMARDs

These medicines may take weeks to months to

become effective.

DMARDs can promote remission.

Chemically synthesised DMARDs:

azathioprine

D-penicillamine

gold salts

methotrexate (MTX)

sulfasalazine (SSZ)


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PROGNOSIS

Disability

Daily living activities are impaired in most

individuals.

After 5 years of disease, approximately 33% of

sufferers will not be working. After 10 years, approximately half will have

substantial functional disability

Mortality

Estimates of the life-shortening effect ofRA vary;

most sources cite a lifespan reduction of 5 to 10

years

RA sufferers suffer a doubled risk.

Rheumatoid Arthritis Presentation

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